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Hyperlipidemia, pharmacology Slide 1 Hyperlipidemia, pharmacology Slide 2 Hyperlipidemia, pharmacology Slide 3 Hyperlipidemia, pharmacology Slide 4 Hyperlipidemia, pharmacology Slide 5 Hyperlipidemia, pharmacology Slide 6 Hyperlipidemia, pharmacology Slide 7 Hyperlipidemia, pharmacology Slide 8 Hyperlipidemia, pharmacology Slide 9 Hyperlipidemia, pharmacology Slide 10 Hyperlipidemia, pharmacology Slide 11 Hyperlipidemia, pharmacology Slide 12 Hyperlipidemia, pharmacology Slide 13 Hyperlipidemia, pharmacology Slide 14 Hyperlipidemia, pharmacology Slide 15 Hyperlipidemia, pharmacology Slide 16 Hyperlipidemia, pharmacology Slide 17 Hyperlipidemia, pharmacology Slide 18 Hyperlipidemia, pharmacology Slide 19 Hyperlipidemia, pharmacology Slide 20 Hyperlipidemia, pharmacology Slide 21 Hyperlipidemia, pharmacology Slide 22 Hyperlipidemia, pharmacology Slide 23 Hyperlipidemia, pharmacology Slide 24 Hyperlipidemia, pharmacology Slide 25 Hyperlipidemia, pharmacology Slide 26 Hyperlipidemia, pharmacology Slide 27 Hyperlipidemia, pharmacology Slide 28 Hyperlipidemia, pharmacology Slide 29 Hyperlipidemia, pharmacology Slide 30 Hyperlipidemia, pharmacology Slide 31 Hyperlipidemia, pharmacology Slide 32 Hyperlipidemia, pharmacology Slide 33 Hyperlipidemia, pharmacology Slide 34 Hyperlipidemia, pharmacology Slide 35
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Hyperlipidemia full review
Definition, Classification &
All hyperlipidemic drugs mechanism of action

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Hyperlipidemia, pharmacology

  1. 1. Hyperlipidemia Presented by ; Mohd siraj Guided by Prof . Abdul hadi sultan prof . Mohd zubair
  2. 2. 1. Definitions 2. Classification 3. Mechanism of actions
  3. 3. Hyperlipidemia : Abnormally elevated level of lipid in blood, these lipids can adhere to the walls of the arteries and restrict blood flow which creates significant risk of heart attack and stroke There are 3 major lipids in our blood Cholesterol Triglycerides Phospholipids
  4. 4. Cholestrol : which is necessary for the synthesis of bile acid. Triglycerides : which provides energy to the cell. Phospholipids : which is the major component of cell membrane .
  5. 5. Lipid produces in liver. From liver lipids not able to move to blood stream because they are insoluble in blood plasma . So, liver raps protein around the lipid resulting in new molecule called lipoprotein Lipoprotein move to blood stream through out the body
  6. 6. Types of lipoprotein : Very low density lipoprotein Low density lipoprotein High density lipoprotein
  7. 7. Very low density lipoprotein (VLDL) It composed of low level of protein , & high level of cholesterol & triglyceride Protein cholesterol Triglycerides
  8. 8. Low density lipoprotein (LDL) It composed of only protein and cholestrol. It is also known as bad cholestrol. Protein Cholesterol
  9. 9. High density lipoprotein (HDL) : It composed of more amount of protein and very less amount of cholestrol. It is also known as good cholestrol Protein Cholestrol Triglyceride
  10. 10. Firstly liver releases VLDL in blood stream VLDL provides triglyceride to various cell for function . After utilizing triglyceride VLDL becomes LDL which contain only Protein and cholestrol. LDL provides cholestrol to various cell which required .
  11. 11. If our body makes too much LDL , it will deposited to the walls of artery causing a fat material called plaque. Due to which narrow blood vessel thereby reduce blood flow , that’s why they are called bad cholestrol.
  12. 12. Liver also makes HDL that removes excess of cholestrol from cells and plaque , and returns excess cholestrol to liver that’s why they are called good cholestrol.
  13. 13. classification
  14. 14. Drug used to lower lipid levels : HMG-CoA reductases inhibitors Fabric acid derivatives Niacin (nicotinic acid) Bile acid sequestrates Cholesterol absorption inhibitors
  16. 16. Mechanism of action
  17. 17. HMG CoA REDUCTASE INHIBITOR : HMG-CoA Mevalonic acid Cholesterol HMG-CoA Mevalonic acid Cholesterol HMG CoA REDUCTASE Inhibit the enzyme HMG-CoA reductase , which Is the rate limiting step in cholesterol synthesis. In liver cell HMG CoA REDUCTASE
  18. 18. Decrease LDL, Increase HDL , Decrease triglyceride. The drugs which inhibit HMG CoA reductase enzyme includes : Atorvastatin Fluvastatin Lovastatin Pravastatin Rosavastatin Side effects : liver toxicity , muscle toxicity.
  19. 19. Nicotinic acid Triglycerides Fatty acid Harmone sensative lipase Fatty acids Triglyceride VLDL ADIPOSE TISSUE LIVER
  20. 20. Normally , Harmone sensative lipase is responsible for break down of triglyceride to fatty acids in adipose tissue. These fatty acids is used by liver to makes its own triglyceride then become important component of VLDL
  21. 21. Nicotinic acid Triglycerides Fatty acid Harmone sensative lipase Fatty acids Triglyceride VLDL ADIPOSE TISSUE LIVER
  22. 22. To decrease VLDL production NICOTINIC ACID Inhibit harmone sensative lipase . Increase HDL , decrease LDL , decrease triglycerides The drug which inhibit harmone sensative lipase is NIACIN . Side effects : Skin flushing , hyperglycemia, And hepatotoxicity
  23. 23. PPAR α PPAR α Fibrate Fibrate FIBRATES Fibrates work primarily by activating nuclear transcription receptor called PPAR α (Peroxisome proliferator activated receptor alpha).
  24. 24. PPAR α is found in metabolically active tissues such as liver and adipose tissue Binding of fibrates to PPAR α induces activation or inhibition of certain proteins involved in lipid metabolism. which ultimately decrease in the production of LDL and VLDL . The drugs belongs to this class include FINOFIBRATE GEMFIBRIZIL SIDE EFFECTS : GI distubance , rhabdomyolsis have been reported in patients with impared renal function
  25. 25. BILE ACID SEQUESTRANTS : As we know bile acid are made from cholestrol . Liver produce bile acid and stored in the gall bladder, and they excreted into the gut where they facilitate digestion & absorption of lipid preventing the reabsorption of bile acid
  26. 26. This increase in bile acid excretion in turn creates increase demand for their production Now bile acid sequestrants basically binds with bile acid and salt in the small intestine the formation of this insoluble complex prevents the reabsorption of of bile acids and thus lead to their excretion BILE ACID SEQUESTRANT + BILE ACID = FORMS A COMPLEX
  27. 27. Since bile acid are made from cholesterol liver cell increase their number of LDL receptors to bring in more LDL cholestrol in order to meet this new demand so the end result is decreased levels of circulating LDL The drugs belongs to this class include CLESEVELAM, COLESTIPOL , CHOLESTYRAMINE SIDE EFFECTS : constipation nausea are the common side effects
  28. 28. CHOLESTEROL ABSORPTION INHIBITORS Under normal condition Mechanism of cholesterol absorption in small intestine Free cholesterol that comes either from bile or dietary sources first binds to protein abbreviated NPC1L1 which is located in the plasma membrane of the cells known as enterocytes that lines the intestinal walls .
  29. 29. Upon endocytosis the cholesterol is released and the NPC1L1 return back to the plasma membrane This Binding then triggers endocytosis which utilizes protein complex called clathrin AP2 that works on the cell membrane to internalize the cholesterol cargo upon
  30. 30. Now the cholesterol absorption inhibitors simply binds to NPC1L1 and inhibits its ability to intract with clathrin AP2 complex that is necessary for endocytosis this lead to decreased dilevery of intestinal cholesterol to the liver Which in turn causes decrease in hepatic cholesterol level & ultimately increased clearance of LDL cholesterol from the circulation
  31. 31. EZETIMBE
  32. 32. The side effects of ezetimibe are mild and few which makes it a good choice for patients with intolarant or unresponsive to statins . Currently the only drug belongs to this class is EZETIMBE
  33. 33. THANK YOU
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Hyperlipidemia full review Definition, Classification & All hyperlipidemic drugs mechanism of action


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